by Ivo Tarfusser, MD (©1996)
In conclusion, in my opinion, our current view of "chronic prostatitis" is too narrow and rigid, the presuppositions are too limited, leading to the present incapacity to expand knowledge. Several researchers in the field are now looking closely at possible mechanisms causing prostatitis (CBP, NBP) to live ist own life, i e factors resulting from an initial inflammatory process (alterations of micro-membranes in the glands, antigene-antibody-deposits, auto-immune mechanisms, etc) which act as irritant, further enhancing the inflammatory reaction. Others are still busy searching for a hypothetical, yet undiscovered microorganism responsible for NBP. Few, if any, are dealing with the issue of PDy.
It seems very unlikely that there is one single organ or mechanism responsible for the different manifestations of the chronic prostatitis syndrome (or chronic pelvic syndrome). Rather, we should consider there being many different etiologies leading to the same or similar symptoms, through a variety of different pathogenetic mechanisms. Since the symptoms are similar, slovenly labeled "prostatitis", there is a tendency to ask for the cause of prostatitis. I am afraid that we will never get an answer as long as we, obstinately, think of prostatitis as a disease confined to the prostate or as one nosologic entity, instead of appreciating these symptoms as being the consequence of one among several potential causes and mechanisms, not necessarily emanating from the prostate or from the prostate alone.
Conventional, generally accepted, assessment methods, like cultures etc, are certainly indispensable, and will deliver an indication about the possible origin of complaints in a subset of patients. But we cannot limit our efforts to these techniques, nor should attention in research be exclusively directed to the prostate. This will, inevitably, lead to having a large number of patients without explainable cause of their condition.
One important step in thinking in different tracks has been the effort at some major American centers (Mayo, Stanford) in focusing on the role of the pelvic floor muscles. In my opinion, extending this concept to an understanding of the interaction between periphery (prostate, bladder, seminal tract), pelvic floor musculature and, probably very important, the pudendal nerve (which carries sensibility and motoric signals to the interested area) will yield a better understanding of the symptoms in another subset of patients. It seems reasonable that the symptoms in the pudendal nerve innervation area, in a part of the patients, is generated in the periphery, by inflammatory/infectious disease of the prostate, irritation of parts of the seminal tract, etc. But it is also conceivable (and should be investigated) that other patients get their symptoms from a primary irritation of the nerve (compression, mechanical irritation), leading to similar manifestations as in prostatitis. Finally, a dynamic interaction between these mechanisms could be postulated: patients in whom the process starts in the periphery, causing reflectory pelvic floor hypertension which in turn starts a vicious circle of pudendal nerve irritation, eventually becoming an independent self-perpetuating mechanism, even after remission/cure of the original peripheral affection. To emphasize the problem, the investigating community is faced with, one has to remind himself that any combination of pain and urogenital symptoms can, theoretically, be caused both by primary disease in the periphery as well as primary/secondary neuropathy, with or without myopathy.
Also regarding pathologic conditions in the secondary sex glands, themselves, we should take other mechanisms into consideration than merely trying to detect hypothetical infectious agents. It seems highly unlikely that mechanisms dominating pathogenetics in other organ systems (like the urinary tract, gastro-intestinal tract, etc), e g obstruction, should not be determinant in many cases in the seminal tract and the prostate, too. I admit, it is difficult to prove scientifically due to the lack of appropriate investigative methods (invasive or, preferably, non-invasive ones), but it should not be too difficult to get indirect evidence. In analogy to similar pathology elsewhere in the body, in a glandular organ system consisting essentially of microtubes and small channels, passed by fluid of varying composition and viscosity, obstruction has to be suspected as one main pathogenetical mechanism until proved otherwise. And treatment should be directed to relieve obstruction, even if our diagnostic tools are too coarse to allow aquisition of a 100% diagnosis. In many patients with prostatodynia, I found that pressure on the seminal vesicles can elicit the pain the patients seeks help for. In my opinion, when present, this finding suggests prostatodynia representing a pathologic condition in the seminal tract, often involving the seminal vesicles. These glands have never got the right attention, due to their hidden position, usually not reachable by the examiner's finger at DRE. In most cases, I found changes in the seminal vesicles suggestive of obstruction, with the cause of the obstruction lying down-streams, in the narrow ejaculatory ducts. Like the ureter, these ducts have physiological segments which are even narrower then the rest of the duct (the openings into the urethra), where stones, inspissated seminal fluid, cellular detritus can get stuck and cause that colicky pain so characteristic for many patients with prostatodynia. This can also happen, if the ejaculatory ducts are compressed or distorted from out-side (completely or partially, reversibly or permanently) by inflammatory edema, utricular cysts, BPH or cancer. Finally, the inflammatory wall reaction which may ensue can lead to cicatriceal stenoses or obturation of the duct. Whether the seminal vesicle and the deferential duct can overcome the increased resistance by increasing the force of peristaltic contractions or, eventually, decompensate and get dilated from back-pressure, the result is often pain (again: compare what happens in the urinary, biliary and intestinal tract in the case of ostruction). The analogies with other organ systems are so evident that it amazes me that they have not yet been translated to the seminal tract, providing ideas for research in this area. As elsewhere in the body, obstructed organs are exquisitely prone to secondary infection and inflammatory reaction, even if obstruction is not always necessary to start inflammation/infection. On the other hand, inflammation/infection will readily resolve in a well-drained organ with therapy; if, however, obstruction persists, inflammation/infection will hardly be coped with, even by intensive long-term drug treatment. Does'nt this make us think of the difficult therapeutical situation we are faced with when treating longstanding "prostatitis"? The undeniable therapeutic efficacy of well-performed prostatic massage, in some cases, is probably due to this draining effect. In selected cases, especially severe ones, it is my experience that surgical procedures can provide relief or cure, like it does in any other part of the body affected by obstruction and/or focal chronic inflammatory processes and/or abscesses.
In my experience, a key to a better diagnosis is the exact analysis of the symptoms. Ejaculatory pain, especially if one-sided, often yields a finding of obstruction in the seminal tract. Burning sensation at micturition combined with painful ejaculation should direct attention to the junction of the urinary and seminal tract (veru). Hematospermia not rarely discloses a utricular cyst. Pain related to prolonged sitting, biking, truck-riding, especially in absence of other uro-genitary symptoms, may suggest a closer investigation/palpation of the pudendal nerve (neuropathy?) and pelvic floor muscles. Crucial in such investigation is a thorough palpation with the finger and the TRUS-probe, and a morphological evaluation (TRUS). Nonetheless, there will still remain a group of patients without detectable cause, but in cases with severe pain, chasing the location of maximal pain will most often disclose a cause with a reasonable degree of reliability.
I would like to summarize my postulations and suggestions as follows:
In any case, we have to get more distance to and question current concepts, we have to change our big picture radically by introducing elements by now neglected or underestimated. Without doubt, some elements of conventional diagnostic methods and treatment options are still valuable, but they have to be brought into a wider context and their role has to be re-evalued, in any case, we should question and relativize their central role as "state-of-the-art" methods. Otherwise we'll discover ourselves standing on the same spot for another twenty years.
Ivo Tarfusser, MD
Go to: